998 resultados para Impurity effect
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Double Degree. A Work Project, presented as part of the requirements for the Award of a Master’s Degree in Finance from NOVA – School of Business and Economics and a Masters Degree in Management from Louvain School of Management
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based on the report for the Doctoral Conference of the PhD programme in Technology Assessment, held at FCT-UNL Campus, Monte de Caparica, July 2013. The PhD thesis has the supervision of Dr. Salomé Almeida (Central Hospital of Lisbon), and co-supervision of Prof. Manuel Ortigueira (FCT-UNL).
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INTRODUCTION: Antibiotic-associated diarrhea (AAD) is an important side effect of this specific class of drugs. The objective of this study was to investigate the effect of the use of probiotics in the treatment of AAD. METHODS: A group of hospitalized patients, who contracted diarrhea during or after 7 days of suspension of antimicrobial medication, was blindly randomized to receive a standardized diet associated with the use of the probiotics (Lactobacillus casei and Bifidobacterium breve) or its corresponding placebo, three times a day. RESULTS: Seventy patients were studied. For the experimental (n=35) and control (n=35) groups, respectively, the average time of treatment was 5.06±2.18 and 5.49±3.17 days (p=0.95), and the average duration of diarrhea, among those who were healed, was 4.87±2.13 and 4.52±2.55 days (p=0.36). Four (11.4%) patients who received probiotics and ten (28.6%) who received the placebo were not cured (p=0.13), and relapse rates were similar between both groups. Seven patients from each group, in addition to diarrhea, presented cases of bloating and/or abdominal cramps and/or vomiting (p=1.00). CONCLUSIONS: In this light, it is concluded that L. casei associated with B. breve, in the administered dosage and frequency, has no effect on the antibiotic-associated diarrhea. Similar studies need to be conducted with higher doses of these or other probiotics.
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INTRODUCTION: Governador Valadares is an endemic area of American tegumentary leishmaniasis (ATL). The detection rate was 15.36 per 100,000 habitants from 2001 to 2006 (Miranda, 2008). This study aimed to analyze the effects of age on the frequency of adverse reactions caused by antimony in the treatment of ATL in the City of Governador Valadares, State of Minas Gerais, Brazil, during 2009. METHODS: Data were collected from the forms of the Information System for Notifiable Diseases, and from charts, questionnaires, and home visits to patients. RESULTS: The study included 40 patients, 26 (65%) of whom were males. Individuals over the age of 50 had a 66% higher rate of adverse effects than subjects who were 50 years old or less (CI 95%, 1.14-2.41). The average age of individuals who reported some type of adverse effect was 44.11 years (SD = 20.14), while the average age of the group that did not report any adverse effect was of 25.46 years (SD = 18.37; p < 0.01). Clinical healing was 67.5%, and 10% of patients discontinued the treatment. CONCLUSIONS: In the treatment of ATL, the age of patients should be considered, because most adverse reactions occur in individuals over 50 years of age. For this reason, the drug should be used with restriction in these cases.
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Organizations are undergoing serious difficulties to retain talent. Authors argue that Talent Management (TM) practices create beneficial outcomes for individuals and organizations. However, there is no research on the leaders’ role in the functioning of these practices. This study examines how LMX and role modeling influence the impact that TM practices have on employees’ trust in their organizations and retention. The analysis of two questionnaires (Nt1=175; Nt2=107) indicated that TM only reduced turnover intentions, via an increase in trust in the organization, when role modeling was high and not when it was low. Therefore, we can say that leaders are crucial in the TM context, and in sustaining a competitive advantage for organizations.
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Double degree
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RESUMO: A isquémia cerebral é uma das doenças mais predominantes a nivel mundial, sendo uma das principais causas de mortalidade e invalidez. Parte da propagação de dano no cérebro é causado por inflamação descontrolada, causada principalmente por disfunção da microglia. Desta forma, existe a necessidade de tentar desenvolver estratégias para melhor compreender e modular as acções destas células. O monóxido de carbono (CO), é uma molécula endógena com provas dadas como anti-neuroinflamatório em vários modelos. Assim, o principal objectivo do trabalho foi o estudo do CO como um modulador da acção da microglia, com principal foco dado à comunicação entre estas células e neurónios, tentando entender se existe um efeito neuroprotector por inibição da inflamação. Um protocolo de meio condicionado foi estabelecido usando as linhas celulares BV2 e SH-SY5Y, de microglia e neurónio. A molécula CORM-A1, que liberta expontaniamente CO, foi usada como método de entrega da molécula às celulas. Demonstrámos que o pre-tratamento de células BV2 com CORM-A1 gera neuroprotecção já que reduz a morte celular de neurónios SH-SY5Y quando são incubados com meio condicionado de microglia activada em conjunto com o pró-oxidante t-BHP (tert-butil hidroperóxido). Assim, considerámos que o CO promove neuroprotecção ao inibir as acções inflamatórias da microglia. O papel anti-inflamatório da molécula CORM-A1 foi confirmado quando se verificou que pré-tratamento desta molécula em microglia BV2 limita a secreção de TNF-α mas estimula a secreção de IL-10. Por último, a CORM-A1 induziu a expressão do receptor da microglia CD200R1, molécula que participa na comunicação neurónio-microglia e fundamental para a modulação das acções inflamatórias destas últimas. Em suma, o nosso trabalho reforçou as propriedades anti-neuroinflamatórias do CO e uma capacidade de modular viabilidade neuronal através do seu efeito a nível de comunicação célula-célula. ---------------------------- ABSTRACT: Brain ischemia is a widespread disease worldwide, being one of the main causes of mortality and permanent disability. A portion of the damage that ensues following the ischemic event is caused by unrestrained inflammation, which is mainly orchestrated by exacerbated microglial activity. Hence, developing strategies for modulating microglial inflammation is a major concern nowadays. The endogenous molecule carbon monoxide (CO) has been shown to possess anti-neuroinflammatory properties using in vitro and in vivo approaches. Thus, our objective was to study CO as modulator of microglial activity, in particular in what concerns their communication with neurons, by promoting neuronal viability and limiting inflammatory output of activated microglia. A conditioned media strategy was established with BV2 microglia and SH-SY5Y neurons as cell models. CO-releasing molecule A1 (CORM-A1), a compound that releases CO spontaneously, was used as method of CO delivery to cells. We found that CORM-A1 pre-treatment in BV2 cells yields neuroprotective results, as it limits cell death when SH-SY5Y neurons are challenged with conditioned media from LPS-activated microglia and the pro-oxidant t-BHP (tert-butyl-hydroperoxide). Thus, we assumed carbon monoxide promotes neuroprotection via inhibition of microglial inflammation, displaying a non-cell autonomous role. CORM-A1 pre-treatment limited inflammation by inhibiting BV2 secretion of TNF-α and stimulating IL-10 production. These results reinforce that CO’s anti-inflammatory role confers neuroprotection, as the alterations in these cytokines occur concurrently with the increase in SH-SY5Y viability. Finally, we showed for the first time that carbon monoxide promotes the expression of CD200R1, a microglial receptor involved in neuron-glia communication and modulation of microglia inflammation. Further studies are necessary to clarify this role. Altogether, other than just highlighting CO as an anti-inflammatory and neuroprotective molecule, this work set the foundation for disclosing its involvement in cell-to-cell communication.